scholarly journals A cell culture model of the blood-brain barrier.

1991 ◽  
Vol 115 (6) ◽  
pp. 1725-1735 ◽  
Author(s):  
L L Rubin ◽  
D E Hall ◽  
S Porter ◽  
K Barbu ◽  
C Cannon ◽  
...  

Endothelial cells that make up brain capillaries and constitute the blood-brain barrier become different from peripheral endothelial cells in response to inductive factors found in the nervous system. We have established a cell culture model of the blood-brain barrier by treating brain endothelial cells with a combination of astrocyte-conditioned medium and agents that elevate intracellular cAMP. These cells form high resistance tight junctions and exhibit low rates of paracellular leakage and fluid-phase endocytosis. They also undergo a dramatic structural reorganization as they form tight junctions. Results from these studies suggest modes of manipulating the permeability of the blood-brain barrier, potentially providing the basis for increasing the penetration of drugs into the central nervous system.

2006 ◽  
Vol 109 (3-4) ◽  
pp. 233-244 ◽  
Author(s):  
Nicola F. Fletcher ◽  
David J. Brayden ◽  
Brenda Brankin ◽  
Sheila Worrall ◽  
John J. Callanan

2004 ◽  
Vol 998 (2) ◽  
pp. 218-229 ◽  
Author(s):  
Victoria I. Inglis ◽  
Michael P.J. Jones ◽  
Arthur D.Y. Tse ◽  
Alexander S. Easton

2000 ◽  
Vol 21 ◽  
pp. 86
Author(s):  
Siobhan M. Brennan ◽  
Lawrence T. McGrath ◽  
Stephen P. McIlroy ◽  
Peter A. Passmore

2003 ◽  
Vol 161 (3) ◽  
pp. 653-660 ◽  
Author(s):  
Takehiro Nitta ◽  
Masaki Hata ◽  
Shimpei Gotoh ◽  
Yoshiteru Seo ◽  
Hiroyuki Sasaki ◽  
...  

Tight junctions are well-developed between adjacent endothelial cells of blood vessels in the central nervous system, and play a central role in establishing the blood-brain barrier (BBB). Claudin-5 is a major cell adhesion molecule of tight junctions in brain endothelial cells. To examine its possible involvement in the BBB, claudin-5–deficient mice were generated. In the brains of these mice, the development and morphology of blood vessels were not altered, showing no bleeding or edema. However, tracer experiments and magnetic resonance imaging revealed that in these mice, the BBB against small molecules (<800 D), but not larger molecules, was selectively affected. This unexpected finding (i.e., the size-selective loosening of the BBB) not only provides new insight into the basic molecular physiology of BBB but also opens a new way to deliver potential drugs across the BBB into the central nervous system.


1996 ◽  
Vol 270 (4) ◽  
pp. H1149-H1158 ◽  
Author(s):  
L. Descamps ◽  
M. P. Dehouck ◽  
G. Torpier ◽  
R. Cecchelli

A cell culture model of the blood-brain barrier consisting of a coculture of bovine brain capillary endothelial cells (BBCECs) and astrocytes has been used to examine the mechanism of iron transport to the brain. Binding experiments showed that BBCECs express 35,000 high-affinity (concn at 50% receptor saturation = 11.3 +/- 2.1 nM) transferin (Tf) receptors per cell. In contrast to apo-transferrin (apoTf) we observed a specific transport of holo-transferrin (holoTf) across BBCECs. This transport was inhibited completely at low temperature. Moreover, the anti-Tf receptor antibody (OX-26) competitively inhibited holoTf uptake by BBCECs. Pulse-chase experiments demonstrated that only 10% of Tf was recycled to the luminal side of the cells, whereas the majority of Tf was transcytosed to the abluminal side; double-labeling experiments clearly demonstrated that iron crosses BBCECs bound to Tf. No intraendothelial degradation of Tf was observed, suggesting that the intraendothelial pathway through BBCECs bypasses the lysosomal compartment. These results clearly show that the iron-Tf complex is transcytosed across brain capillary endothelial cells by a receptor-mediated pathway without any degradation.


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